GBM tumor cells exhibit or readily acquire invasive capabilities, allowing them to quickly spread throughout the brain. Growing evidence indicates that they co-opt innate pathways that allow neural progenitor and related stem-like cells to spread throughout the brain during development and wound healing. In doing so, they take immediate advantage of the diverse molecular and mechanical substrates that facilitate cell movement along central nervous system (CNS), blood vessel and white matter tracts. Standard-of-care treatments aggressively combine maximal surgical resection, radiation, and chemo/immunotherapy, but all typically fail due to GBM tumor cell plasticity and motility. Understanding and regulating these adaptive mechanisms is thus critical to improved treatments and patient outcomes. Since surgery can deal well with the bulk of the tumor, and chemotherapy/radiation can overcome most proliferating cells, our focus is to develop approaches to regulate and control the motile cells that quickly spread within the brain. Questions that we can address using our methods are: where do GBM cells spread over time and space in a given patient? How does this differ in patients with different initial conditions? How do different treatments affect this dispersion? What treatments could regulate motility? How can the plasticity and adaptation abilities of GBM cells be reduced?